Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pathologic studies were done on 20 hearts of patients who had typical clinical signs and symptoms of Kawasaki disease. The cardiac lesions were classified according to the duration of illness at the time of death. Stage I (zero to nine days) was characterized by acute perivasculitis and vasculitis of the microvessels (arterioles, capillaries, and venules) and small arteries, and acute perivasculitis and endarteritis of the three major coronary arteries (MCAs). Pericarditis, myocarditis, inflammation of the atrioventricular conduction system, and endocarditis with valvulitis were also present. Stage II (12 to 25 days) was characterized by panvasculitis of the MCAs and aneurysm with thrombus in the stems. Myocarditis, coagulation necrosis, lesion of the conduction system, pericarditis, and endocarditis with valvulitis were also present. In stage III (28 to 31 days), granulation of the MCAs and disappearance of inflammation in the microvessels were noted. Patients in stage IV (40 days to 4 years) had scarring with severe stenosis in the MCAs. Fibrosis of the myocardium, coagulation necrosis, lesions of the conduction system, and endocardial fibroelastosis were also present. The features observed revealed Kawasaki disease to be acute and inflammatory. The angiitis begins in the microvessels and fibrinoid necrosis of the media is rare. The disease is one with a pathologic pattern previously unknown.
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PMID:Pathology of the heart in Kawasaki disease. 26 36

A young man with nonsyphilitic keratitis and vestibulo-auditory dysfunction (Cogan's syndrome) and a recurrent febrile illness has been observed over a 10 year period. The systemic manifestations have included a splenic abscess vasculitis, pericarditis, aortic valvulitis, and mono-articular inflammatory arthritis.
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PMID:Cogan's syndrome with arthritis and aortic insufficiency. 74 53

We reviewed the autopsy material of 169 patients with rheumatoid arthritis (RA) and studied the cardiac changes is these patients. Systemic vasculitis was observed in 26 cases (15.38%) among 169 patients with RA. In 17 cases (10%) we found vasculitis of the subepicardial and/or intramural coronary vessels. Coronary arteritis or arteriolotis has led to multifocal small, and/or large myocardial infarctions in 10 cases (5.9%) and was the cause of progressive cardiac insufficiency, the direct cause of death. Multifocal circumscribed myocardial infarction reported in rheumatoid disease. In 8 cases rheumatoid nodules were found in the myocardium, 3 of them related to vasculitis. We suggest that rheumatoid nodules are the most severe form of necrotizing granulomatous vasculitis. Pathognomic nodular rheumatoid pericarditis was seen in 3 cases and diffuse rheumatoid pericarditis in another case. Pathognomic nodular valvulitis was found in 7 cases. Rheumatoid nodules localized to the epi-, myo-, or endocardium were observed on 9 patients. Generalized secondary amyloidosis was observed in 32 (18.93%) of the 169 patients with RA. Secondary amyloidosis was prevalent in the heart in 29 of 32 cases (relative frequency: 90.62%).
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PMID:Cardiac changes in rheumatoid arthritis. 136 61

Described in this paper are pathomorphological alterations to the heart postmortem recorded from 100 deceased with rheumatoid arthritis. Vasculitis of subepicardial or intramural rami of coronary arteries was recorded from twelve cases and had caused multiple myocardial necrosis in ten of these. These developments had led to progressive cardiac insufficiency which actually then was the direct cause of death. Formal pathogenesis of vasculitis-related multifocal myocardial necrosis in concomitance with rheumatoid arthritis had never been described in the literature before, although such reference would have been justified for the clinical consequences for which it deserves to be emphasised as a nosological entity in its own right. Isolated rheumatic nodes were detected in the myocardium of five of the decreased and could be attributed to rheumatic arteritis in two cases. Those myocardial rheumatic nodes, according to the author's view, represent the severest form of necrotising rheumatic vasculitis. Pathognomonic pericarditis was found in four cases (2 pericarditis nodularis and 2 pericarditis rheumatica). Pathognomonic nodular valvulitis was identified in another four cases. Systemic secondary amyloidoses were found to be present in 24 of the above 100 deceased with chronic polyarthritis. The heart was involved in 23 of these 24 cases (95.8%).
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PMID:[Heart alterations in chronic polyarthritis]. 176 83

Cogan's syndrome is a rare syndrome manifested by nonsyphilitic interstitial keratitis and audiovestibular symptoms including hearing loss, tinnitus, and vertigo. Systemic manifestations may occur. Systemic vasculitis and aortic insufficiency secondary to aortitis and valvulitis are two of the most serious manifestations.
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PMID:Vasculitis and Cogan's syndrome. 218 59

A clinico-morphological observation of Wegener granulomatosis in a 29-year-old man is described. The disease started with the gastrointestinal disorders followed by lung and renal disturbances which dominated. Heart enlargement and systolic-diastolic noise in the Botkin point were found. Infectious endocarditis with a complex aortal defect were diagnosed. The patient died 6 months later. The autopsy revealed a necrotizing lung granulomatosis, disseminated vasculitis, renal and spleen infarcts. Vasculitis with granulomatosis, destructive changes in the intima were found in the supravalvular part of the aorta and at the base of the aortic valve as well as severe fibrinous valvulitis.
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PMID:[A case of Wegener's granulomatosis with involvement of the aortic valve]. 262 66

A 40 year old man with a history of myocardial infarction and hypertension presented with transient cerebral ischaemic attacks, aortic regurgitation, a raised erythrocyte sedimentation rate, and thrombocytopenia. The anticardiolipin syndrome was diagnosed and he was treated with prednisolone and warfarin. He died two years later after the development of acute heart failure. At necropsy his heart showed widespread arteriolar thrombosis without vasculitis, recanalised large vessel occlusion, and a "post-inflammatory" valvulitis of the aortic valve.
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PMID:Findings at necropsy in the heart of a patient with anticardiolipin syndrome. 275 75

Aortitis as a feature of rheumatoid arthritis is considered rare. We have, however, identified 10 patients with aortitis from among 188 consecutive autopsy cases of rheumatoid arthritis. There were 5 men and 5 women with a mean duration of rheumatoid arthritis of 9.6 years. Nine were rheumatoid factor positive and had associated nodules. In addition to standard treatment regimens, 9 patients received corticosteroids. Although involvement of the thoracic aorta was most common, involvement of both the thoracic and abdominal aorta was present in 4 cases. Two patients had aneurysmal dilatation of the thoracic aorta and 1 of the abdominal aorta. Microscopic features of aortitis included necrosis of medial smooth muscle and elastica, with an inflammatory infiltrate comprising primarily lymphocytes and plasma cells. A panmural aortitis was seen in 3 cases. Rheumatoid granulomas were noted in the aortic wall in 5. The diagnosis of aortitis was not made until autopsy in any case. Aortitis was hemodynamically significant in 3 patients. Two had congestive heart failure secondary to thoracic aortitis and aortic valvulitis, and 1 had rupture of an abdominal aortic aneurysm at a site involved by aortitis. Seven patients had rheumatoid vasculitis with a mean of 10 organs involved. Six of these died of complications directly related to vasculitis, including 4 patients with coronary arteritis and associated myocardial infarction. Aortitis can be a feature of severe rheumatoid arthritis and is often associated with rheumatoid vasculitis. Hemodynamic compromise does occur and may be fatal.
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PMID:Rheumatoid aortitis: a rarely recognized but clinically significant entity. 292 41

Plant pathologists have known for several years that intracellular Mollicutes (M), i.e. cell wall deficient bacteria, are plant vascular pathogens, but because those M are non-cultivatable, they can only be studied by Transmission Electron Microscopy (TEM). Only recently have similar M been shown to be human and animal pathogens. Those human ocular Vasculitis (V) and mouse chronic ocular and lethal systemic V producing M parasitize vitreous polymorphonuclear leucocytes, lymphocytes, and monocytes as 'viral-like' 0.005-0.010 micron elemental particles which grow within the leucocyte into 0.01-0.03 micron diameter tubules, 0.3-1.5 micron spherules, and distinctive 0.5-0.7 micron cocci with spore-like cell walls. This report describes the 48 arteriolar and capillary sized V, Aschoff nodules, valvulitis, and myocytolytic lesions in the heart and great vessels in 18 of 100 human vitreous VM containing eyelid inoculated mice versus 0 of 200 controls (P less than 0.05) plus VM within parasitized leucocytes in 15 of 15 of those lesions by TEM. The results indicate dissemination of VM from the eyelid to produce a significant incidence of distinctive multifocal VM directly induced cardiovascular micro-V lesions that probably contributed to their excessive mortality. Because several human idiopathic diseases develop similar cardiovascular lesions a TEM search for VM parasitized leucocytes in those human diseases seems justified.
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PMID:Mouse lethal cardiovascular disease: induction by human leucocyte intracellular Mollicutes. 337 65

We reviewed the medical records and autopsy reports of 50 patients with systemic lupus erythematosus to determine the clinical and neuropathological features of this disease. Neuropsychiatric disturbances were found in the majority (74%) of the patients, occurring as psychiatric illness only (5 patients), neurological disorders only (15 patients), and both together (17 patients). Central nervous system (CNS) lesions were present in half the patients; embolic brain infarcts (10 patients) and CNS infections (8 patients) were the most common. Cardiac sources of emboli were Libman-Sacks endocarditis (5 patients), chronic valvulitis (2 patients), and left side of heart mural thrombus (2 patients). There was no evidence of active CNS vasculitis. Clinical features of thrombotic thrombocytopenic purpura (TTP) developed during the terminal illness in 14 patients, 7 of whom also had pathological evidence of TTP. Correlation between neuropsychiatric disorders and brain lesions could be made in approximately half the patients. This study indicates that cardiac emboli from Libman-Sacks endocarditis and TTP are common pathogenetic factors of CNS disease in systemic lupus erythematosus, whereas CNS vasculitis is rare.
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PMID:Clinical and neuropathological findings in systemic lupus erythematosus: the role of vasculitis, heart emboli, and thrombotic thrombocytopenic purpura. 338 74


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